Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipoprotein lipase was purified from bovine milk and labeled with 125I. After intravenous injection to rats the labeled lipase rapidly disappeared from the blood. The initial half-life was about 1 min and more than 70% of the radioactivity was found in the liver at 10 min. 30 min after the injection about 10% of the injected radioactivity was present in acid-soluble form in blood, indicating that the enzyme had been rapidly degraded. Injection of asialofetuin, ribonuclease B or mannan in amounts known to block the hepatic receptors for glycoproteins with exposed galactose, N-acetylglucosamine or mannose residues did not retard the removal of the lipoprotein lipase. Thus, some other, as yet undefined, receptor is implicated. Lipoprotein lipase is known to bind to heparin and some related polysacchrides. Heparin injected before the enzyme delayed its removal and heparin injected after the enzyme caused an immediate increase in blood radioactivity, signifying return from tissues to blood of labeled enzyme. Lipoprotein lipase is present at the endothelium in several extrahepatic tissues and is rapidly turned over. Its presence in blood in appreciable amounts would cause a derangement of lipid transport. The efficient hepatic removal of the enzyme may thus serve an important physiological purpose in keeping the blood levels of this enzyme low.
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PMID:Rapid removal to the liver of intravenously injected lipoprotein lipase. 9 43

The changes in the individual glycosaminoglycans of the aorta and in lipoprotein lipase activity of the aorta, liver and heart have been studied at various stages in the development of mild atheroma in the rat. Three responses were seen: (a) Hyaluronic acid initially decreased, then increased; (b) Heparan sulphate and chondroitin sulphates A and C initially increased, then decreased. (c) Chondroitin sulphate-B and heparin increased with progressing lipid infiltration and decreased markedly only in the later stages. Ageing changes were also investigated in the rat aorta: total cholesterol, phospholipids and triglycerides increased progressively from weaning to 9 months of age. Hyaluronic acid decreased after weaning, reached a minimum at 6 months and then increased thereafter. Heparan sulphate and chondroitin sulphate-C reached a maximum at 6 months and then decreased thereafter. Chondroitin sulphates A and B showed a similar but less marked pattern of change with age. Heparin progressively increased with age. Aortic lipoprotein lipase activity increased in the early stages of atheroma and then decreased as the lipid infiltration became more severe. The ageing study showed that enzyme activity was quite high at weaning. decreased considerably at 3 months, but thereafter fell only slightly.
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PMID:Changes in aortic glycosaminoglycans and lipoprotein lipase activity in rats with age and atheroma. 12 74

Hypertriglyceridemia, a risk factor for premature atherosclerosis, may result from decreased use of plasma triglycerides by tissues. The removal of triglycerides is mediated by the enzyme lipoprotein lipase (LPL). Heparin releases LPL from tissues and post-heparin plasma lipolytic activity (PHLA) has been extensively used to elucidate the mechanism of hypertriglyceridemia in various diseases. There is evidence to show that postheparin plasma contains enzymes other than LPL. Hence data on total PHLA are difficult to interpret. Availability of assays for the LPL component of PHLA has clarified equivocal findings in certain hypertriglyceridemic states. However, the LPL component is also heterogeneous. The LPL "isoenzymes" from various extrahepatic tissues behave differently under various metabolic conditions. Therefore, to understand properly the LPL system it is necessary to study the specific tissue LPL. Furthermore, the serum activator for LPL is now characterized. Its importance is evidenced by the recent discovery of a hypertriglyceridemic patient deficient in this apoprotein.
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PMID:The lipoprotein lipase system: new understandings. 20 4

Heparin-releasable lipoprotein lipase (LPL) activity was measured in biopsy samples of adipose tissue and skeletal muscle of 8 normal healthy females, first during an isocaloric diet and then after 2 and 7 days on a 400-kcal diet. In adipose tissue the LPL activity expressed per tissue weight fell to 38% and to 22% of the initial level after 2 and 7 days' caloric restriction, respectively. In skeletal muscle the LPL activity rose slightly after two days (+24%) but decreased to 49% of the initial value after seven days on diet. The estimated total body LPL activity decreased to 50% and to 20% of the baseline value after 2 and 7 days, respectively, but the relative contribution of skeletal muscle to the total LPL increased from 10 to 30%. The triglyceride and VLDL triglyceride concentrations were not significantly changed during the low calorie diet but the LDL triglyceride increased and the HDL cholesterol decreased significantly (P less than 0.01). It is concluded that substantial restriction of calorie intake results in a decrease of over-all triglyceride removal capacity but in an increase of the fraction removed by skeletal muscle. The decrease of HDL cholesterol is probably a consequence of the low turnover of exogenous and endogenous triglyceride-rich lipoproteins.
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PMID:Effects of caloric restriction on lipid metabolism in man: changes of tissue lipoprotein lipase activities and of serum lipoproteins. 22 89

We measured lipoprotein lipase activity in dried defatted preparations of rat lung using doubly labeled chylomicron triglyceride as substrate. The enzyme activity was linear for the first hour of incubation at 37 degrees C, had a pH optimum of 8.1 and was completely inhibited by 0.5 M NaC1. Lungs from fed rats hydrolyzed chylomicron triglyceride at a rate of 13.00 mumoles/g per h; the activity rate was unchanged by fasting 8-72 h. Heparin infusion into isolated lungs caused immediate release of lipoprotein lipase to the venous effluent. The activity released was equivalent to about 10% of total lung lipoprotein lipase activity in both fed and fasted rats. Since the ability to remove blood triglyceride is directly related to the level of lipoprotein lipase activity, these findings indicate that the lung is one of the few tissues able to remove efficiently blood triglyceride during fasting.
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PMID:Lipoprotein lipase in rat lung. The effect of fasting. 23 20

Published studies have shown that overproduction of very low density lipoproteins is a major factor leading to hypertiglyceridemia in obesity. Few systematic studies of triglyceride removal or postheparin lipoprotein lipase activity (LPLA) in obesity have appeared. We have examined heparin-released lipoprotein triglyceride hydrolase activities in 12 lean and 12 obese age- and sex-matched volunteers after overnight fasting. Heparin doses were calculated to compensate for the disproportionality between body mass and plasma volume in obesity. Triglyceride hydrolase activities of hepatic (HTGLA) and extrahepatic (LPLA) origin were distinguished by in vitro inhibition of LPLA with protamine sulfate. Incremental heparin doses were given to each subject to determine lipase activities under conditions of maximal release and to define sensitivity to heparin-facilitated lipase release. Maximal postheparin LPLA and HTGLA (u/ml plasma or u/total plasma vol) were similar in lean and obese individuals despite a nearly three-fold increase in calculated adipose tissue mass in the obese. Since adipose tissue LPLA has been reported to increase in proportion to adipocyte size, the lack of difference in maximal postheparin LPLA was expected. There was an inverse correlation between plasma triglyceride concentration and LPLA/kg adipose tissue. These empirical observations may reflect relatively decreased heparin-releaseable (functional) LPLA in relation to adipose organ mass in obese subjects. The mechanism of this relationship has not been established.
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PMID:Postheparin plasma lipase activities in obesity: failure to increase with adipose organ enlargement. 68 71

Heparin-like glycosaminoglycans (GAG) were isolated from commerical Vessel and their biologic properties studied. Vessel was found to be a mixture of chondroitin sulfates, dermatan sulfate and heparin-like GAG. Chondroitin sulfates and dermatan sulfate in Vessel were hydrolyzed by chondroitinase ABC and the residual Vessel was fractionated on a Dowex-1 Cl- column eluting with a stepwise-increasing concentration of NaCl (1.2--4.0 M). The major fractions eluted at 1.6 M and 1.8 M NaCl were tentatively identified by chemical analysis as heparin-like GAG with somewhat lower sulfate content than standard heparin. Both fractions had lipoprotein lipase-releasing activity and anticoagulant activity similar to heparin, but 1.6 M NaCl fraction had a third of the anticoagulant activity of standard heparin. The 1.8 M NaCl fraction complexed with serum lipoproteins similarly to heparin. In preliminary studies cholesterol-fed rabbits treated with Vessel exhibited somewhat less atherosclerosis than controls.
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PMID:Studies of glycosaminoglycan composition and biologic activity of Vessel, a hypolipidemic agent. 72 39

Fourteen normal dogs received continuous infusions of intravenous heparin for one year by means of an implantable infusion pump. Heparin wad admistered at an overall mean rate of 666 units/kg/day, a dose sufficient to prolong the Lee-White clotting time to greater than twice normal. Eight control, animals, under the same dietary and activity regimen, received continuous infusions of bacteriostatic water for one year by means of implanted pumps. Serum cholesterol concentrations rose to 50% above control values after one month of heparin infusion, and remained significantly (P less than 0.05) elevated at this level for the remaining 11 months. Serum triglyceride levels were unchanged. A possible mechanism for this elevation resides in the known effect of heparin to increase plasma free fatty acid concentrations by its activation of lipoprotein lipase. These results may have implications for the long-term use of heparin anticoagulation in the treatment of atherosclerotic states in man.
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PMID:The effect of continuous heparin infusion for one year on serum cholesterol and triglyceride concentrations in the dog. 83 45

Release of lipoprotein lipase from rat fat cells incubated at 20 degrees in medium with albumin, but without glucose proceeded at a constant rate for 30 min. The initial rate of release was increased when serum was present in the medium. Maximal stimulation (100-300%) was produced with 3.8% serum. The maximal increment in release caused by serum was always greater than that produced by heparin and when both were added release was greater than it was with either one alone. The active component(s) of serum, nondialyzable and stable for 30 min at 56 degrees C, was present in sera from humans and rats in the fed or fasted state. Glucose plus insulin (but neither alone) enhanced the rate of lipase release in the presence of serum but not in its absence. The half-life of the lipase in basal medium of 20 degrees C was 90 min. Heparin decreased this to about 50 min and serum markedly prolonged it whether or not heparin was present. Lipoprotein lipase activity in cells and fractions thereof was assayed in extracts of acetone powders. After centrifugation of fat cell homogenates at 600 times g for 15 min, only 50-60% of the activity was recovered in the supernatant. After centrifugation at 100 000 times g for 60 min, the supernatant contained about 10% of the total activity and the sediment 40%. In some experiments, most of the rest was recovered in the floating fat fraction. Total lipoprotein lipase activity of cells plus medium increased steadily during incubation of fat cells for 1h at 30 degrees C. The major increment occurred in the cells and activity in the medium was always less than 15% of the total. Our observations are consistent with the view that activation may be an important determinant of fat cell lipoprotein lipase activity as well as an integral part of the release process.
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PMID:Release of lipoprotein lipase from fat cells in vitro. 112 15

There was a positive correlation in normal man between heparin releasable lipoprotein lipase and lipoprotein lipase of ammonium hydroxide homongenate of acetoneether powder in adipose tissue. Heparin releasable as lipoprotein lipase activity was about twice as high as the enzymatic activity in acetone powder, even though 40-70% of the original activity remained in the tissue after incubation with heparin. This might indicate that activation of the enzyme is associated with its release by heparin from tissue. The lipoprotein lipase activity per unit weight and per fat cell were affected differently by obesity: In obese subjects lipoprotein lipase per unit weight was propotionally lower than the activity per fat cell. The expression of activity per fat cell appears to avoid the effect of obesity, and hence increased fat cell size, on values obtained.
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PMID:Human adipose tissue lipoprotein lipase: comparison of assay methods and expressions of activity. 112 69


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